Fat but Fit? Not Likely.
Metabolically healthy obese status is likely a transient condition where weight management is required to prevent the establishment of unhealthy cardiometabolic features. Weight loss, but not gains in cardiorespiratory fitness after exercise-training, predicts improved health risk factors. Although fitness is certainly important (and can improve/temper health risk factors to an extent), the number one indicator of improved cardiometabolic risk factors is weight loss. Believing that seemingly normal cardiometabolic blood levels alone are a case for “fit” is erroneous logic in itself.
Research has shown that, more often than not, it is only a matter of time before degradation of joints, cancer occurrence, cardiovascular disease onset, loss of blood glucose control, and the formation of many other chronic health conditions occurs if body fat is not lost.
In the research referenced above:
•MetS health improvements were associated with body weight losses rather than with CRF increases.
•Clinical advice should emphasize body weight loss in exercise programs.
One hundred sixty middle aged (54 ± 8 years; 50% women) individuals with metabolic syndrome, with body mass index (BMI) of 32 ± 5 kg m−2 completed this study. Metabolic syndrome (MetS) was defined as the presence of three of the following five risk factors: elevated waist circumference, blood pressure, fasting blood glucose, blood triglycerides, or reduced HDL-C. Exclusion criteria included untreated cardiovascular or renal disease, or any condition associated with exercise intolerance.
Supervised aerobic interval training (43 min per session) with a frequency of three times per week during 16 weeks were performed. Maximal aerobic capacity (VO2MAX) was assessed on an electronically-braked cycle ergometer (Ergoselect 200, Ergoline, Germany) during a graded exercise test using breath by breath indirect calorimetry (Quark b2, Cosmed, Italy) to measure O2 consumption and CO2 production. Heart electrical activity was continuously monitored using a 12 lead ECG (Quark T12, Cosmed, Italy).
A separate study using resistance training bolstered the findings of the title study by showing fat loss was more effective for cardiometabolic health than muscle gain. “Reductions in fat mass predicted increases in HDL cholesterol, insulin sensitivity index, and decreases in waist circumference. In contrast, increases in lean mass did not predict changes in any of the measured cardiometabolic health indices.” The findings continued: “Health improvements with training that emphasize resistance exercises are typically attributed to increases in lean mass; however, these results underscore reducing body fat to predict cardiometabolic health improvements.”
“Body mass index (BMI), waist circumference (WC), percentage of fat mass (BF%), fat-mass index (FMI), and waist-to-height ratio (WHR) were included as body fatness measurements. A high cardio-metabolic risk cluster was derived by assessing triglycerides, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, fasting glucose, and blood pressure. In both sexes, higher levels of all fatness parameters were associated with increased cardio-metabolic risk. Combined analysis showed that unfitness (lower normalized grip strength) and high fat had the highest cardio-metabolic risk odds ratio for waist circumference and fat-mass index in men and women, respectively.”
Metabolically healthy obese status is likely a transient condition where weight management is demanded to prevent the establishment of unhealthy cardiometabolic features. Over half of the participants in this study (ATTICA study: 1514 men and 1528 women (aged >18 years old) free of CVD and residing in the greater Athens area, Greece) who were deemed “metabolically healthy obese” transitioned to cardiovascular disease or metabolic disorder onset within 10 years.
The literature persuasively suggests that the accumulation of pro-inflammatory cells, in the adipose tissue of obese patients, through cytokines and extracellular vesicles, accelerates the rate of aging both in the adipose tissue itself and the entire organism. Mitochondrial dysfunction occurs in aged tissues, in response to excessive nutrient intake, and in obesity, contributing to inflammation and insulin resistance. Aging and obesity appear superimposable in their impact on mitochondria and it is reasonable to hypothesize that they could exert additive effects. Obesity significantly decreases mechanisms associated with proteome maintenance. There appears to be a strong relationship between obesity and senescence. There is solid evidence that obesity deregulates cellular mechanisms related to nutrient sensing.
“Metabolically healthy obese individuals are associated with an increased risk of cardiovascular diseases.”
“Obesity is a convincing risk factor for 11 types of cancer.”